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10.1038/ncomms6914 http://scihub22266oqcxt.onion/10.1038/ncomms6914 C4293039!4293039!25574809     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 298.79999999999995 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Nat+Commun 2015 ; 6 (ä): 5914 Nephropedia Template TP {{tp|p=25574809|t=2015. Vasculopathy associated hyperangiotensinemia mobilizes hematopoietic stem cells/progenitors through endothelial AT2R and cytoskeletal dysregulation |pdf=|usr=}}{{25574809}} gab.com Text Vasculopathy associated hyperangiotensinemia mobilizes hematopoietic stem cells/progenitors through endothelial AT2R and cytoskeletal dysregulation JO: Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=25574809 #FOAvip Patients in organ failure of vascular origin have increased circulating hematopoietic stem cells and progenitors (HSC/P). Plasma levels of angiotensin II (Ang-II), are commonly increased in vasculopathies. Hyperangiotensinemia results in activation of a very distinct Ang-II receptor set, Rho-family GTPase members, and actin in bone marrow endothelial cells (BMEC) and HSC/P, which results in decreased membrane integrin activation in both BMEC and HSC/P, and in HSC/P de-adhesion and mobilization. The Ang-II effect can be reversed pharmacologically and genetically by inhibiting Ang-II production or signaling through BMEC AT2R, HSCP AT1R/AT2R or HSC/P RhoA, but not by interfering with other vascular tone mediators. Hyperangiotensinemia and high counts of circulating HSC/P seen in sickle cell disease (SCD) as a result of vascular damage, is significantly decreased by Ang-II inhibitors. Our data define for the first time the role of Ang-II HSC/P traffic regulation and redefine the hematopoietic consequences of anti-angiotensin therapy in SCD. Twit Text FOAVip Vasculopathy associated hyperangiotensinemia mobilizes hematopoietic stem cells/progenitors through endothelial AT2R and cytoskeletal dysregulation ????Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=25574809 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25574809 #FOAvip English Wikipedia <ref>{{Cite pmid|25574809}}</ref> Vasculopathy associated hyperangiotensinemia mobilizes hematopoietic stem cells/progenitors through endothelial AT2R and cytoskeletal dysregulation #MMPMID25574809 Chang KH; Nayak RC; Roy S; Perumbeti A; Wellendorf AM; Bezold KY; Pirman M; Hill SE; Starnes J; Loberg A; Zhou X; Inagami T; Zheng Y; Malik P; Cancelas JA Nat Commun 2015[]; 6 (ä): 5914 PMID25574809show ga Patients in organ failure of vascular origin have increased circulating hematopoietic stem cells and progenitors (HSC/P). Plasma levels of angiotensin II (Ang-II), are commonly increased in vasculopathies. Hyperangiotensinemia results in activation of a very distinct Ang-II receptor set, Rho-family GTPase members, and actin in bone marrow endothelial cells (BMEC) and HSC/P, which results in decreased membrane integrin activation in both BMEC and HSC/P, and in HSC/P de-adhesion and mobilization. The Ang-II effect can be reversed pharmacologically and genetically by inhibiting Ang-II production or signaling through BMEC AT2R, HSCP AT1R/AT2R or HSC/P RhoA, but not by interfering with other vascular tone mediators. Hyperangiotensinemia and high counts of circulating HSC/P seen in sickle cell disease (SCD) as a result of vascular damage, is significantly decreased by Ang-II inhibitors. Our data define for the first time the role of Ang-II HSC/P traffic regulation and redefine the hematopoietic consequences of anti-angiotensin therapy in SCD. äVasculopathy associated hyperangiotensinemia mobilizes hematopoietic s(epmc).pdf DeepDyve Pubget Overpricing